This study aimed to assess the effects of simulated microgravity (SMG) on bovine muscle satellite cells (bSCs). The results demonstrated that bSCs maintained a fibroblast-like morphology throughout SMG exposure from day 3 to day 7. However, cells in the SMG group exhibited reduced proliferation compared to the control group, as indicated by lower cell density at both time points. In contrast, cell viability was higher in the SMG group than in the control group. Cell cycle analysis revealed a higher proportion of SMG-treated bSCs in the G0/G1 phase and a lower proportion in the S phase at day 3, suggesting cell cycle arrest at an early stage. Interestingly, by day 7, the percentage of cells in the S phase increased in the SMG group and exceeded that of the control group, indicating a partial recovery of proliferative activity. Western blot analysis showed decreased expression of key cell cycle-related proteins, including cyclin A1/A2, cyclin D1, and CDK2, in SMG-treated cells compared to controls at the early stage. Notably, cyclin D1 and CDK2 expression levels were upregulated at the later stage under SMG conditions. Additionally, nuclear morphology in SMG-treated bSCs displayed enlargement and irregularity. Overall, these findings suggest that SMG initially suppresses bSC proliferation by inducing cell cycle arrest, but cells can partially retrieve their proliferative capacity at later stages, potentially through upregulation of cell cycle regulatory proteins.
To explore the ameliorating effect of treadmill exercise on depression-like behavior in rats with chronic unpredictable stress (CUS). Thirty-six Sprague-Dawley rats were divided into three groups (n=12 per group): a control group, a CUS group and a CUS+exercise (CUS+EX) group. The CUS and CUS+EX groups received a 4-week CUS treatment, and the CUS+EX group began a 4-week moderate-intensity treadmill exercise at the second week of CUS treatment. Following the CUS treatment and treadmill exercise, the depressive-like behavior of rats was assessed using the open field test (OFT) and tail suspension test (TST). Plasma melatonin levels were measured using an enzyme-linked immunosorbent assay, and the superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels in the prefrontal cortex (PFC) were detected using commercial kits. Compared with the control group, the CUS group showed shortened latency to first immobility and prolonged total immobility time in the TST, and decreased time spent in the center and reduced crossing and vertical activities in the OFT. Additionally, the SOD activity and the protein expressions of sirtuin 1 (SIRT1) and nuclear factor E2 associated factor 2 (Nrf2) in the PFC decreased, whereas the MDA level increased in the CUS group. Four weeks of concurrent treadmill exercise attenuated the effects of CUS: compared with the CUS group, the CUS+EX group exhibited reduced depressive-like behaviors, prevention of the CUS-induced decline in PFC SOD activity and SIRT1/Nrf2 protein expression and attenuation of the CUS-induced increase in PFC MDA levels. Treadmill exercise concurrently increased plasma melatonin levels and activated the SIRT1/Nrf2 antioxidant pathway in the PFC, which may contribute to the observed improvement in depressive-like behavior.
Excessive osteoclast activity drives bone-resorptive disorders, and oxidative stress is a key regulator of osteoclast differentiation. Hydrogen sulfide (H?S), an endogenous antioxidant, may modulate this process, but its mechanisms remain unclear. In this study, RANKL (50 ng/mL) was used to induce osteoclastogenesis in RAW264.7 cells, with or without the H?S donor sodium hydrosulfide (NaHS; 50-200 ?M). Osteoclast formation was evaluated by TRAP staining and NFATc1/Cathepsin K expression, while oxidative stress, lipid peroxidation, mitochondrial function, and ferroptosis-related parameters were assessed. Mechanistic studies revealed that NaHS promoted Nrf2 nuclear translocation and upregulated GPX4, HO-1, and NQO1, whereas inhibition of Nrf2 or GPX4 partially reversed these effects. NaHS significantly suppressed osteoclast differentiation, alleviated oxidative stress, and restored mitochondrial function. These findings demonstrate that H?S inhibits RANKL-induced osteoclastogenesis via the Nrf2/GPX4 pathway and suggest this redox axis as a potential therapeutic target for bone-resorptive diseases.
Sepsis is a complicated disorder caused by infection, which may trigger various symptoms. Lipopolysaccharides (LPS) are among the primary pathogens which can stimulate host's immunoreaction. In the late stage of sepsis, the patients' immune system is significantly suppressed, thus the mortality increases. Notably, autophagy is pivotal during sepsis, in which autophagosome-lysosome fusion mediated by syntaxin 17 (STX17) is a key step. Previous studies have shown that histone deacetylase 2 (HDAC2) deacetylated STX17 to promote autophagosome-lysosome fusion. Trichostatin A (TSA) as a HDAC inhibitor (HDACi) has the capability of inhibiting histone deacetylase activity, while such an effect can be reversed by ITSA-1. This time LPS was used to stimulate human monocyte-macrophages (THP-1 cells) to establish the inflammatory cell model. TSA and ITSA-1 were administrated. The cell proliferation was examined by WST-1. Cytokines such as TNF-? and IL-6, as well as HDAC2 activity and deacetylated STX17 (DA-STX17) expression were detected by ELISA. Also, autophagy-related proteins such as P62 and microtubule-associated protein light chain 3 (LC3) were detected by Western Blotting (WB), and autophagosome-lysosome fusion was observed by fluorescence assay. Cell apoptosis was measured by flow cytometry. Besides, network pharmacology analysis was conducted. The data showed that TSA inhibited HDAC2 activity, and remarkably downregulated DA-STX17 expression, accompanied by the lower expression of P62 and LC3 ?/I. Decreased DA-STX17 promoted autophagosome-lysosome fusion, and inhibited TNF-? secretion. Furthermore, network pharmacology analysis revealed an inner relationship concerning HDAC2 between TSA and sepsis. Therefore, TSA can be considered a potential drug to cure sepsis-related diseases.
Despite the widespread use of silver nanoparticles (AgNPs) in consumer, industrial, and biomedical products, their potential effects on female reproductive health, particularly during critical developmental periods, remain insufficiently understood. The present study was therefore designed to investigate in vivo the dose-dependent effects of AgNP exposure on ovarian function and reproductive health in pubertal female rats. Pubertal Wistar albino female rats were divided into control and two AgNP groups (0.05 and 0.50 mg/kg/day). After one month of therapy, the females in the different groups were euthanized, and ovarian samples were collected. The results indicated that administration of AgNPs significantly increases the number of primordial follicles and significantly increases the number of growing follicles. Western blot analysis revealed that aromatase (Cyp19) and proliferating cell nuclear antigen (PCNA) were upregulated in both treatment groups. Similarly, the number of mRNA transcripts associated with folliculogenesis and steroidogenesis increased significantly in the high-dose treatment group. In addition, the level of growth differentiation factor 9 (GDF9) mRNA increased significantly in a dose-dependent manner. However, the levels of anti-Müllerian hormone (Amh) mRNA were considerably higher in the low-dose group and lower in the high-dose group, demonstrating that the detailed regulation of this gene is affected by AgNP dose. Analysis of the phosphatidylinositol 3-kinase signaling pathway revealed that compared to a 0.05 mg/kg, a AgNP exposure at 0.5 mg/kg significantly enhanced the PI3K/AKT/mTOR pathway and impacted Ampk signaling in a distinct manner. These findings suggest that AgNPs increase follicular development and deplete the follicular reserve, resulting in a phenomenon known as “burnout”.
Lung collapse and ventilation heterogeneity are common in mechanically ventilated critically ill patients. Electrical impedance tomography (EIT) enables real-time bedside monitoring of regional ventilation and may facilitate individualized respiratory management. This study evaluated the effect of EIT-guided respiratory muscle training (RMT) combined with postural adjustment on lung recruitment in patients with respiratory failure. In this single-center, prospective, randomized controlled trial, 150 patients were randomly assigned to three groups: the EIT collaborative group (EIT-guided RMT+postural adjustment), the EIT posture group (EIT-guided positioning only), and the conventional collaborative group (RMT+postural adjustment without EIT). The primary endpoint was the change in end-expiratory lung impedance (EELI). Secondary outcomes included oxygenation, respiratory mechanics, ventilation homogeneity, and clinical outcomes. Data were analyzed using ANOVA and linear mixed-effects models. The interventions were applied for up to 5 consecutive days after randomization or until ICU discharge, whichever occurred first. After 5 days, EELI increased by 18.4±7.6 % in the EIT collaborative group, which was significantly greater than the increases observed in the EIT posture group (9.1±6.2 %) and the conventional collaborative group (3.7±5.8 %) (P<0.001). CL % decreased markedly without a significant increase in OD %, while CoV and GI index indicated improved ventilation uniformity. The EIT collaborative group also showed favorable trends toward improved oxygenation and respiratory mechanics, along with shorter ventilation duration and higher extubation success rates. A significant interaction between EIT supervision intensity and intervention level was confirmed (F=6.45, P=0.011). No serious adverse events occurred. These findings suggest that EIT-guided RMT combined with postural adjustment may enhance lung recruitment and ventilation homogeneity, with potential benefits for respiratory mechanics and selected short-term clinical outcomes. Real-time EIT feedback may provide a safe, individualized strategy for respiratory rehabilitation in critically ill patients.
Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a major cause of cirrhosis, liver cancer, and cardiovascular disease. Early mitochondrial dysfunction drives lipid imbalance, inflammation, and fibrosis. Given the lack of approved pharmacological treatments, this study compares the mitochondria-targeted agents MitoQ and SS-31 for their effects on mitochondrial function, oxidative stress, apoptosis, and inflammation in aged, nutritionally stressed mice with MASLD. Aged female C57BL/6 mice (12-14 months) were fed a high-fat, high-fructose diet for 16 weeks to induce MASLD. Mice were randomized into four groups: (i) control diet, (ii) MASLD, (iii) MASLD + MitoQ (25 mg/kg/day, oral), and (iv) MASLD + SS-31 (3 mg/kg/day, i.p.). Liver tissues were analyzed by western blotting for mitochondrial biogenesis and dynamics markers (PGC-1?, NRF1, and TFAM), oxidative stress regulators (SOD2, Nrf2, 4-HNE), apoptosis-related proteins (Bax, and Bcl-2), inflammatory and fibrotic mediators (NF-?B, and NLRP3), and insulin signaling proteins (p-Akt, and GLUT2). Both MitoQ and SS-31 significantly improved mitochondrial protein expression and overall liver health compared with untreated MASLD mice. MitoQ primarily enhanced mitochondrial antioxidant defenses by upregulating SOD2 and Nrf2 while decreasing 4-HNE adduct formation, reflecting reduced oxidative damage. SS-31, in contrast, more effectively preserved mitochondrial structural integrity. Both compounds attenuated inflammation by suppressing NF-?B and NLRP3 activation. They also improved insulin sensitivity by increasing p-Akt and GLUT2 expression. Histological analysis using H&E staining revealed marked reductions in hepatic steatosis. Mitochondrial dysfunction drives MASLD progression. In aged MASLD mice, MitoQ enhances antioxidant defense, SS-31 preserves integrity, and both improve insulin signaling and reduce fibrosis, supporting mitochondrial therapy for MASLD.
This study investigated the effects of sodium butyrate (SB) supplementation on milk fat synthesis in lactating goats fed a high-concentrate (HC) diet. Twelve lactating Saanen goats were randomly allocated into two groups: a control group (HG) fed a HC diet (concentrate-to-forage ratio = 60:40), and a SB-treated group (SG) fed the same basal diet supplemented with 10 g/kg SB. Compared with the HG group, SB supplementation significantly increased milk fat percentage and milk fat yield (P < 0.01). Meanwhile, SB significantly decreased lipopolysaccharide (LPS) concentrations in both jugular and mammary vein plasma (P < 0.05). In addition, SB enhanced mammary antioxidant capacity, as indicated by elevated activities of superoxide dismutase (SOD) (P < 0.01) and total antioxidant capacity (T-AOC) (P < 0.05). Global metabolomic analysis (UPLC MS/MS) of mammary gland tissues identified 558 differential metabolites, of which 50 were significantly altered and mainly enriched in amino acids, benzene derivatives, heterocyclic compounds, and fatty acids. Pathway analysis showed that SB significantly activated the pentose phosphate pathway, glycerophospholipid metabolism, and linolenic acid metabolism. Furthermore, mammary gland triglyceride (TG) content was significantly higher in the SG group than in the HG group (P < 0.05). SB also upregulated the mRNA expression of key lipogenic enzymes, including acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) (P < 0.05). These findings demonstrate that SB improves mammary gland health and mitigates the adverse effects of HC diets on milk quality by enhancing de novo fatty acid synthesis in the mammary gland of lactating goats.
Solasodine (SOL) is a steroidal glycoalkaloid that shows a wide range of biological effects, most notably anticancer activities. Eryptosis is the programmed cell death of erythrocytes that leads to anemia. Specifically, chemotherapy-induced anemia can be precipitated in part by eryptosis triggered by anticancer agents. We hypothesize that the cytotoxic effects of SOL observed in cancer cells are nonspecific and extend to human erythrocytes. Eryptosis following SOL exposure was detected by fluorescence-assorted cell sorting analysis in erythrocytes from healthy volunteers. Phosphatidylserine (PS) translocation and cellular volume were measured using annexin-V-FITC and forward scatter (FSC), respectively. Fluo-4/AM was used to detect cytoplasmic Ca2+ and H2DCFDA was employed to probe oxidative stress. Hemolysis was also assessed by hemoglobin leakage. In addition, different incubation media and inhibitors were tested for their potential influence on SOL activity. Exposure to SOL led to modest but significant hemolysis and was paralleled by significant PS translocation, elevated FSC, and echinocyte morphology. Energy restitution through ATP, guanosine, and adenine significantly reversed PS translocation as did the removal of extracellular Ca2+ and the dissipation of the cell membrane K+ gradient. Co-treatment of erythrocytes with SOL and SB203580, NSC 23766, necrosulfonamide, caffeine, and melatonin significantly inhibited SOL-induced PS translocation. In conclusion, SOL is a novel pro-eryptotic compound whose activity is mediated through energy exhaustion, Ca2+ influx, and cytosolic KCl depletion, and requires p38 MAPK/Rac1 GTPase/MLKL signaling. Metabolic substrates, cation channel modulators, and targeted inhibition provide protective adjuncts to improve the therapeutic index of SOL as it advances toward translational applications.
Preeclampsia (PE) is a pregnancy-specific hypertensive disorder characterized by new-onset hypertension after 20 weeks of gestation, with or without proteinuria, frequently accompanied by systemic arteriolar spasm and dysfunction or injury of multiple organs, including the liver, kidneys, and placenta. This study examined changes in glycolysis- and mitochondria-related gene expression in placental trophoblast cells in PE, aiming to elucidate the role of disrupted energy metabolism in its pathogenesis. A total of 86 pregnant women with singleton pregnancies who received routine prenatal care at the Affiliated Hospital of Hebei University between December 2023 and October 2024 and delivered via cesarean section were enrolled. Among them, 30 patients diagnosed with PE were included in the PE group, and 56 normotensive pregnant individuals were assigned to the control group. General clinical data were collected. The mRNA and protein expression levels of HK2, PKM2, silent information regulator two 1 (SIRT1), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) in placental tissue were measured using real-time quantitative polymerase chain reaction and western blot (WB) analysis. There were no statistically significant differences in maternal age at delivery, body mass index, triglycerides, total cholesterol, or high-density lipoprotein cholesterol between groups (p > 0.5). Significant differences were observed in low-density lipoprotein cholesterol, neonatal birth weight, and 1-minute and 5-minute Apgar scores (p < 0.05). Expression levels of HK2, PKM2, and PGC-1alpha were significantly elevated in placental tissue from the PE group compared to the control group (p < 0.01), while SIRT1 expression was significantly reduced (p < 0.05). Placental tissue from patients with PE demonstrated upregulation of HK2, PKM2, and PGC-1alpha, and downregulation of SIRT1. Dysregulated expression of genes and proteins involved in energy metabolism may contribute to the pathogenesis of PE through impaired trophoblast function.
Atrial inflammation and fibrosis are the pathogenesis of postoperative atrial fibrillation (POAF). It has been reported that invariant natural killer T (iNKT) cells can coordinate tissue inflammation, but whether it can regulate POAF is still unknown. A sterile pericarditis (SP) model was constructed on C57BL/6J mice and Jalpha18-/- mice to simulate POAF. Intraperitoneal injection of anti-interleukin (IL) -6 neutralizing antibody (anti-IL-6) was used for intervention, and atrial fibrillation (AF) was induced by transesophageal sinus atrial node pulse pacing. The levels of iNKT cells and IL-6/signal transducer and activator of transcription 3 (STAT3) signaling pathway were detected by flow cytometry and western blot. HE stain, Masson stain, and immunohistochemistry were used to evaluate the process of inflammation and fibrosis in atrial tissue. The calcium homeostasis and function of atrial mitochondria were evaluated by biochemical detection and fluorescent staining. The expression of iNKT cells was up-regulated in SP mice. The defect of iNKT cells increased the AF induction rate and duration of SP mice, enhanced AF susceptibility, aggravated atrial electrical remodeling, promoted inflammatory cell infiltration and fibrosis, and increased inflammatory factors and fibrotic proteins. Compared with SP mice, iNKT cell defects also aggravated endoplasmic reticulum-mitochondrial calcium coupling disorder, mitochondrial calcium homeostasis imbalance, reduced mitochondrial DNA (mtDNA), adenosine triphosphate (ATP) content, and mitochondrial complex enzyme activity, and increased IL-6 and STAT3 phosphorylation levels. Anti-IL-6 significantly inhibited IL-6/STAT3 signaling pathway, reduced AF induction rate and duration, and improved atrial mitochondrial calcium homeostasis, mitochondrial dysfunction, inflammation, and fibrosis. The deficiency of iNKT cells aggravated atrial tissue mitochondrial dysfunction, inflammation, and fibrosis in POAF mice via activating IL-6/STAT3 axis, and aggravated AF susceptibility.
Pulsed-field ablation (PFA) has become an important non-thermal modality for pulmonary vein isolation in atrial fibrillation (AF), characterized by myocardial selectivity and reduced collateral tissue injury. However, the physiological biomarker response to PFA remains incompletely defined. This study assessed serial changes in myocardial (troponin T, creatine kinase - CK and its isoenzyme - CK-MB) and renal (urea, creatinine) biomarkers in patients undergoing PFA at a single center and compared these findings with current clinical evidence. The study cohort consisted of 52 patients undergoing PFA (73 % men, 27 % women), with 52 % presenting paroxysmal AF and 48 % persistent AF. The mean left atrial diameter was 45 ± 7 mm and the average left ventricular ejection fraction was 55 ± 7 % The mean ablation burden was 67 ± 23 applications per procedure. Biomarkers were measured before and after ablation. Repeated-measures ANOVA demonstrated significant time effects for all myocardial biomarkers (p < 0.001) and significant interactions with ablation burden. Troponin-T increased from near-zero baseline values to markedly elevated levels immediately and 24-hours after the procedure, while CK and CK-MB rose several-fold with only partial decline after the procedure. In contrast, urea and creatinine remained stable, indicating preserved renal function without acute kidney injury. The number of PFA applications correlated positively with late CK and CK-MB values, suggesting that myocardial biomarker load scales with procedural intensity. These findings align with current literature showing extensive myocardial biorelease after PFA but favorable extracardiac safety. By concurrently analyzing myocardial and renal markers, this study demonstrates that substantial biochemical myocardial injury induced by PFA does not translate into measurable renal dysfunction. Overall, PFA appears physiologically consistent with a profile of robust but targeted myocardial injury and preserved renal safety.
Simulation is widely used for training practical skills, clinical procedures, critical thinking, and communication. Its application in teaching cardiovascular physiology represents an innovative educational approach. We introduced the Cardiopulmonary Auscultation Patient Simulator (CPS) "Harvey" into the Physiology curriculum for second-year General Medicine students at Jessenius Faculty of Medicine, Comenius University. During practical sessions, students performed heart auscultation and blood pressure measurement tasks in two ways: classical investigation on each other or working with the CPS simulator in small groups (4-8 students). At the end of the practicals, students completed an anonymous questionnaire evaluating this teaching method. Respondents (n=110; 68 Slovak- and 42 English-program students) perceived the simulation-based teaching very positively. Most students reported that simulations improved their understanding of cardiovascular physiology topics previously covered in lectures. They found the activities easy to perform and expressed interest in broader use of simulation in other sessions. The main limitations reported were insufficient time for repeated practice and the relatively large group size. Students suggested longer sessions and smaller working groups. In conclusion, students considered the simulator-based practicals beneficial for learning and helpful for increasing confidence in practical skills. Based on their feedback, we plan to expand the use of simulations to additional physiology practicals and extend session duration to allow more hands-on practice.
In response to the growing global population and the unsustainable nature of current livestock agriculture, cultivated meat (CM) offers a promising alternative protein source. CM, produced through advanced tissue engineering techniques, aims to mitigate health, ethical, and environmental issues associated with conventional meat. This review evaluates the safety of CM consumption, comparing its risks and benefits to those of traditional meat. CM presents numerous advantages, including the reduction of zoonotic diseases and antibiotic resistance. However, it also introduces new challenges, such as genetic modification concerns and whether the CM can cause any kind of disease of affluence. The review highlights the necessity for rigorous safety assessments and regulatory frameworks to ensure CM's safe integration into the food supply. Additionally, CM production's lower environmental impact, such as low greenhouse gas emissions or reduced land and water use make it a viable solution to global food security and environmental sustainability.
Bioactive peptides generated during probiotic fermentation have emerged as a complex class of food-derived molecules with multifaceted physiological effects relevant to cardiometabolic health. Recent advances in peptidomics, structural analysis, and mechanistic evaluation have revealed that fermentation with lactic acid bacteria, Bacillus species, or mixed cultures produces highly diverse peptide profiles whose activities depend on sequence motifs, hydrophobicity, charge distribution, and resistance to gastrointestinal degradation. These peptides modulate key pathways involved in vascular regulation, glucose metabolism, lipid handling, and inflammatory signaling. Evidence from cellular and animal models consistently demonstrates that selected short sequences inhibit angiotensin converting enzyme, enhance incretin bioactivity through dipeptidyl peptidase IV inhibition, reduce oxidative stress via direct radical scavenging and Nrf2 activation, attenuate inflammatory cascades by neutralizing endotoxin or interfering with immune receptor interactions, and influence lipid metabolism by interacting with bile acids or receptor-regulated transcription factors. Human trials, although heterogeneous in design and outcomes, suggest modest improvements in blood pressure, glucose tolerance, and lipid measures in specific populations, with notable geographical and genetic variability. Controversy remains regarding effect size, reproducibility, and translation of in vitro potency to physiological relevance due to variability in peptide abundance, digestion stability, and differences in habitual diet. Despite such limitations, emerging strategies in controlled fermentation, peptide enrichment, in silico prediction, and combined functional formulations indicate strong potential for targeted development of peptide-rich foods that support cardiometabolic resilience. Continued integration of structural analysis, mechanistic validation, and rigorously designed clinical studies will be essential to clarify their role within food-based preventive strategies.
This study examined the potential of liraglutide to attenuate ferroptosis in an in vitro model of metabolic dysfunction-associated steatotic liver disease (MASLD). HepG2 cells were allocated into three groups: control (Con), free fatty acid (FFA)-treated, and FFA with liraglutide treatment (FFA+LI). After 48 h of treatment, intracellular triglyceride (TG), glutathione (GSH), malondialdehyde (MDA), and iron levels were quantified using commercially available kits. Superoxide dismutase (SOD) activity was also measured. Lipid accumulation was visualized via Oil Red O staining. Expression of ferroptosis-associated genes was assessed through quantitative RT-PCR and western blotting. FFA treatment induced significant lipid accumulation, elevated TG, MDA, and iron levels, and reduced SOD activity and GSH levels compared to the Con group (all p<0.05). Additionally, FFA exposure increased the expression of TFR1 and downregulated SLC7A11, NRF2, and GPX4 (p<0.05 for all comparisons vs. Con). Liraglutide treatment partially reversed these changes, as evidenced by reduced MDA levels and iron content, downregulation of TFR1, and upregulation of NRF2 and GPX4 (FFA+LI vs. FFA, all p<0.05). Liraglutide demonstrated the ability to mitigate lipid accumulation, oxidative stress, and iron overload in HepG2 cells subjected to FFA-induced injury. These effects were associated with modulation of ferroptosis-related gene expression, suggesting a mechanistic basis for the potential protective role of liraglutide in MASLD. Key words Ferroptosis " Free fatty acid " Liraglutide " Metabolic dysfunction-associated steatotic liver disease " Oxidative stress.
Although muscle mass increases during puberty, it plateaus in girls and slowly increases in boys after around 15 years of age. This study investigated the relationship between phase angle and impedance ratio as indicators of muscle quality and age in Japanese individuals aged 15-18 years and examined their relationship with grip strength. Participants included 838 high school, college, or university students (534 boys, 304 girls). Body composition, phase angle, and impedance ratio were measured using a multi-frequency bioelectrical impedance analyzer. Phase angle was calculated from the resistance and reactance to a 50-kHz alternating current, while impedance ratio was calculated from the impedance to 5- and 250-kHz currents. Grip strength was measured using a Smedley dynamometer. Significant effects of age were observed for body size, fat-free mass, grip strength, phase angle, and impedance ratio in the boys. Compared to 16-year-olds, 17-year-olds showed a significantly higher phase angle and significantly lower impedance ratio in whole body, upper limb, and lower limb. In contrast, no significant main effects of age were observed for any of these measures in the girls. Phase angle and impedance ratio were significantly correlated with grip strength at each age in both sexes. These results suggest that phase angle and impedance ratio can be used to assess muscle strength at any age during late adolescence. However, age-specific values may be preferable for boys in late adolescence when using the reference or percentile values for phase angle and impedance ratio. Key words Muscle quality " Muscle mass " Muscle strength " Puberty " Adolescence.
The aim of this study was to determine the effect of rosuvastatin (10 mg/kg/day, p.o.) on the flinching nociceptive behavior produced by subcutaneous injection of 0.5 % formalin in the dorsum of the right hind paw from Wistar rats submitted to a 16-week treatment, including a standard rat chow diet (STD-diet) or a high fat-diet (HF-diet). At three days post-treatment, the formalin-induced nociceptive response was assessed for 1 h. Compared to the STD-diet, the HF-diet significantly increased the number of flinches in the second phase of the formalin test, as well as inducing higher body weight and levels of glucose, total cholesterol, triglycerides, insulin and blood pressure. Rosuvastatin significantly decreased the formalin-induced nociceptive behavior after both diets and significantly reduced those metabolic parameters in rats with a HF- but not STD-diet.
Exercise-induced muscle damage (EIMD) significantly impacts daily work and life. The rapid promotion of repair for EIMD is worthy of attention. This study aimed to investigate the effect and mechanism of microRNAs in treating EIMD. By establishing an acute skeletal muscle injury model, we determined the key time point for skeletal muscle injury repair and the time-specific changes in MRTF-A/Pax7/SRF and muscle regeneration factors during the repair process. MicroRNAs antagonists were injected to verify the targeting relationship between miR-1/133a and MRTF-A/Pax7/SRF. A single bout of acute eccentric exercise caused significant damage to the morphological ultrastructure of rat gastrocnemius muscles, with the most severe injuries occurring 72 h after exercise. At this particular time point, it was identified as crucial for damage repair. Both miR-1-3p and miR-133a-3p collectively targeted and suppressed the protein translation of MRTF-A, Pax7, and SRF. Furthermore, both miR-1-3p and miR-133a-3p antagonists targeted the MRTF-A/Pax7 axis as well as the MRTF-A/SRF axis. MiR-1-3p antagonists primarily promote muscle proliferation and differentiation, while miR-133a-3p antagonists mainly promote differentiation while inhibiting atrophy. Combined injection effectively promote both muscle proliferation and differentiation while inhibiting atrophy, thereby facilitating damage repair in skeletal muscle fiber structure.
This study examined the effects of varying durations of high-fat diet (HFD) exposure on oxidative stress and the NAD+/Sirtuins/PGC1α signaling pathway in rat skeletal muscle. Thirty-two male Sprague-Dawley rats were randomly assigned to either a control group or HFD groups with exposure periods of 4, 8, or 12 weeks. Outcome measures included body weight, inflammatory markers (IL-6, TNF-α, MCP-1), oxidative stress parameters (MDA, SOD, GSH), apoptotic activity, and protein expression levels of key components within the signaling pathway. The results demonstrated that body weight and systemic inflammation progressively increased with the duration of HFD intake. Markers of oxidative stress became significantly elevated by week 8 and further deteriorated by week 12, characterized by increased malondialdehyde (MDA) levels, diminished antioxidant capacity (reduced SOD and GSH), and enhanced apoptosis. A reduction in Sirt3 expression and increased acetylation of PGC1α were detected at 8 weeks, while by 12 weeks, dysregulation extended across the entire NAD+/Sirt1/PGC1α pathway. These alterations were associated with exacerbated oxidative damage. The findings suggest that the duration of HFD exposure plays a critical role in the development of skeletal muscle oxidative stress through progressive and time-dependent impairment of the NAD+/Sirtuins/PGC1α pathway.
